Medication Summary
No standard treatment protocols exist for diffuse toxic goiter; individualization of treatment based on clinical experience is protocol. Patient preference after informed consent affects all therapeutic decisions.
A 2020 literature review that evaluated the strategy of long-term antithyroid drugs versus radioactive iodine or surgery for the management of Graves disease found that long-term antithyroid medications are feasible alternatives to ablative treatments, resulting in euthyroidism with minimal complications and low financial cost, as well as offer advantages regarding quality of life and other outcomes. [17] Individualized decision making remains key.
Beta blockers
Beta blockers should be considered for patients with resting heart rates over 90 bpm or coexistent cardiovascular disease. [1] In symptomatic patients, these drugs decrease the heart rate, systolic blood pressure, muscle weakness, and tremor, as well as improve emotional irritability. Beta blockers may be used during lactation.
Beta blockers are used if symptomatic tremor or palpitations require their use. They may be used even as clinical investigation is ongoing because they have no effect on thyroid gland function, but they block the beta-adrenergic peripheral manifestations of the hyperthyroid state. Propranolol has an effect in decreasing the peripheral conversion of T4 to T3, but this is of unknown clinical significance with the usual doses. The dose may be decreased and then stopped when the euthyroid state occurs. Beta blockers should not be used in the presence of bronchospasm, even the beta1-selective agents. Calcium channel blockers may be substituted.
Iodine
In severe cases of diffuse toxic goiter, such as thyroid storm, iodine in the form of potassium iodide (SSKI) 10 drops twice a day or iopanoic acid 1-3 g per day may be given. These agents inhibit the release of thyroxine from the gland and inhibit peripheral conversion of T4 to T3. They help render a euthyroid state more rapidly in response to antithyroid drugs, or for preparation for surgery, but will eliminate the use of radioiodine for many months due to expansion of the iodine pool and thereby reducing the delivery of radioiodine to the thyroid gland.
Antithyroid agents
Class Summary
These agents may either inhibit hormonogenesis within the thyroid gland or inhibit release of thyroid hormone from the gland.
Propylthiouracil (PTU)
Actively transported into the thyroid gland and inhibits incorporation of iodine to thyroid hormones, and inhibits peripheral conversion of T4 to T3. Drug recommended in pregnancy and lactation with dose adjustment to minimum needed. Laboratory monitoring of free T4 to adjust dose therapy. The serum TSH may lag behind the changes in free T4. Long-term experience with this drug.
Methimazole (Tapazole)
Actively transported in thyroid gland and inhibits thyroid synthesis by preventing oxidation of trapped iodine. Ten times more potent than PTU, and once-a-day dose is effective. Euthyroid state is achieved in 4-6 wk, and maintenance treatment continued for 12-24 mo. Relapse may be observed 1-6 mo after stopping therapy, occasionally later.
Less desirable than propylthiouracil in pregnancy and lactation but may be used if propylthiouracil cannot be used.
Potassium iodide (Pima, Thyro-Block)
Inhibits thyroid hormone secretion. Contains 8 mg of iodide per gtt. May be mixed with juice or water for intake.
May decrease thyroid gland secretion and vascularity for a short time, such as 2 wk; may be used in severe cases of hyperthyroidism, such as thyroid storm, or to prepare patient for thyroidectomy
Supersaturated potassium iodide (SSKI)
Contains 50 mg of iodide per drop. May be mixed with juice or water for ingestion. Inhibits thyroid hormone release.
Corticosteroids
Class Summary
These agents have profound and varied metabolic effects.
Dexamethasone (Decadron)
Steroids block peripheral conversion of T4 to T3. Used as adjunct in management of thyroid storm and symptomatic progressive Graves ophthalmopathy.
Radiopharmaceuticals
Class Summary
These agents are used to destroy thyroid cells.
Radioiodine (I-131)
Agent of choice because it is selectively taken up by the thyroid gland. Causes dysfunction or death of thyroid cells over time. Long-term experience suggests good safety profile.
Beta-adrenergic receptor blockers
Class Summary
Relief of adrenergic symptoms, especially cardiac and neurologic. Propranolol blocks peripheral conversion of T4 to T3, but this is of unknown clinical significance.
Propanolol (Inderal)
Nonselective beta-adrenergic receptor blocker. Also blocks peripheral conversion of T4 to T3. Used along with antithyroid drugs, before and after radioiodine treatment. Useful in thyroid crisis/storm, or in cardiac complications such as atrial fibrillation. Oral or intravenous use controls cardiac and psychomotor manifestations within minutes. Continue until euthyroid state is achieved.
